Creative Touch Permanent Makeup and Aesthetics

Dihydrotestosterone (DHT) is a 5-alpha reduced metabolite of testosterone, produced when 5-alpha reductase enzymes convert testosterone by adding two hydrogen atoms across the 4,5 double bond of the steroid A ring. The result is a molecule that binds the androgen receptor with approximately five times greater affinity than testosterone and dissociates from it more slowly – a potency difference that allows local tissue to amplify androgen signalling substantially without any change in circulating testosterone levels. In skin, this local conversion is the mechanism through which sebaceous glands and hair follicles experience androgen concentrations well in excess of what systemic hormone levels alone would predict. ^[1]

5-Alpha Reductase Isoforms and Their Skin Distribution

Two isoforms of 5-alpha reductase operate in skin with distinct anatomical distributions, and understanding which isoform dominates where clarifies why DHT’s skin effects are site-specific. Type 1 5-alpha reductase is concentrated in sebaceous glands, where its activity is significantly higher in the face and scalp compared to non- acne-prone body sites. It is the primary driver of DHT production for sebum regulation. Type 2 5-alpha reductase localises predominantly to the companion layer of the hair follicle outer root sheath and the granular layer of the epidermis, with additional expression in comedone walls and endothelial cells in inflammatory acne lesions. ^[3] This distribution means that therapeutic targeting of the two isoforms has different clinical consequences: type 1 inhibition is most relevant to sebaceous-driven conditions; type 2 inhibition (finasteride) targets hair follicle miniaturisation more specifically.

Sebaceous Glands and Sebum Production

DHT is the primary androgen driving sebaceous gland activity in facial and scalp skin. Type 1 5-alpha reductase activity in sebaceous glands converts locally available testosterone to DHT, which then activates androgen receptors in sebocytes to promote gland enlargement, sebocyte proliferation, and increased sebum output. This local amplification mechanism explains why sebum production can be dysregulated even in individuals with normal circulating testosterone levels; the relevant variable is intracellular DHT concentration in the gland, not systemic androgen status. ^[2]

Hair Follicle Miniaturisation

DHT’s most clinically recognised skin effect is progressive hair follicle miniaturisation in genetically predisposed scalp follicles – the mechanism underlying androgenetic alopecia (pattern hair loss). DHT binds androgen receptors in dermal papilla cells of susceptible follicles, triggering a cascade that shortens the anagen (active growth) phase and progressively reduces follicle size across successive hair cycles. Terminal hair follicles producing thick, pigmented hair convert through intermediate stages to vellus follicles producing fine, unpigmented hair, and eventually to follicles that cease productive cycling entirely.

The biological paradox – that the same DHT which miniaturises scalp follicles actively promotes growth in beard, body, and axillary hair – is determined by follicle-specific differences in androgen receptor expression and downstream signalling rather than by any difference in DHT itself. Scalp follicles in predisposed individuals are genetically programmed to respond to AR activation with shortened anagen; follicles elsewhere respond with elongated anagen. The hormone is the same; the receptor sensitivity and downstream response differ by anatomical location and genetic background. ^[4] Finasteride (type 2 5-alpha reductase inhibitor) and dutasteride (dual type 1 and 2 inhibitor) address this by reducing DHT availability at the follicle rather than by modifying receptor sensitivity.